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patho unit3 inflammation and repair Cheat Sheet (DRAFT) by

personal exam revision lol

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Acute inflam­ation

Vascular response
1. increase blood flow by vasodi­lation (hista­mine)+ vascular congestion
-> redness, heat
2. increase permea­bility of vessel by retraction and injury
-> edema
3. Lymph flow increase to drain extrav­ascular fluid + secondary inflam­mation

Termin­ations

1. Mediator bursts rapidly due to short half lives e.g. neutrophil
2. Trigger stop signals
- proinf­lam­matory leukot­riene to anti-i­nfl­amm­atory lipoxins
- release anti-i­nfl­amm­atory cytokines

Chemical mediators

Cell-d­erived
Plasma­-de­rived
1. Vasoactive amines
1.Comp­lement system
- Histamine by mast cell
- Inflam­mation
- Serotonin by platelet aggreg­ation
- Opsoni­sation & Phagoc­ytosis
______­___­___­___­___­___­_____
- Cell lysis
2. Arachi­donic acid metabo­lites
______­___­___­___­___­___­_____
Both by leukocyte in lipoxy­genagse pathway
2.Clotting system
Leukot­rienes
- Clotting system: induce thrombin formation
- LTC4,D­4,E4: Vasoco­nst­ric­tion, increase vascular permea­bility
- Kinin system: vasoactive
- Inhibit by LT receptor antagonist
- Complement system
Lipoxins
- Fibrin­olytic system
- Suppress inflam­mation
______­___­___­___­___­___­_____
Prosta­cyclin
3.Kinins
- PGI2, PDI2, PEI2: Vasodi­lation
- form bradykinin
______­___­___­___­___­___­_____
a. increase vascular permea­bility
3.Cyto­kin­es& chemokines
b. non-va­scular smooth muscle contra­ction
Cytokines
c. pain
- Tumor necrosis factor (TNF) & interl­eukin-1 (IL-1)
4. rapidly inacti­vated
a. Increase endoth­elial cell adhesion molecule expression
b. Activation and aggreg­ation of PMN
c. Systemic acute-­phase respon­se:­Fever
Chemokines
- Attract WBC

Chronic inflam­mation

Causes
1. Prolonged inflam­mation
2. Prolonged toxic substance exposure
3. Autoimmune disease

Morpho­logical change

1. Mononu­clear cell infilt­ration (e.g. macrop­hage, lympho­cyte, plasma cell)
2. Cell destru­ction by inflam­matory cells
3. Repair attempts by fibrosis & angiog­enesis

Types of inflam­mation

Granul­omatus inflam­mation
Defective inflam­mation
- Produce granuloma containing an difficult offending agent
-delayed wound healing
- squamo­us>­epi­theloid
Excessive inflam­mation
- fuse> multin­uclear giant cell
- Abnormal reaction of body e.g. allergy
 
- Fibrosis & tissue injuries

Scar formation steps(­Con­nective tissue deposi­tion)

1. Angiog­enesis
2. Granul­ation tissue formation
3. Connective tissue remode­lling'

Cutaneous wound healing(1)

- Clean wound, only epithelial layer
Inflam­matory phase
1. Formation of blood clot
- Neutrophil appears after 24hrs
- Proteo­lytic enzyme to clean out debris and invading bacteria
Prolif­erative phase
1. Formation of granul­ation tissue
- Induction of fibroblast and endoth­elial cell prolif­eration
- Composed of newly formed thin capill­aries & loose ECM also
- Peak at day5
- To cover the wound
2. Angiog­enesis
i. VEGF >Va­sod­ila­tio­n& I+perm­eab­ility
ii. Proteo­lytic degrad­ation of parent vessel BM>> capillary sprout
iii. Migration of endoth­elial cells toward angiog­enetic stimulus
iv. Prolif­eration of endoth­elial cell behind leading edge of migrating cells
v.Matu­ration of end. cells into capillary tubes
vi. Recrui­tment of perien­dot­helial cells for mature vessel
3.Cell prolif­eration and collagen deposition
- Macrophage replace neutro­phils after 48hrs (key cellular consti­tue­nts> main resource for chemokines & GF)
- Migration and prolif­eration of fibroblast at injury site > secrete and deposit collagen
- Epithelial cells prolif­erate to centre of wound
Remodeling phase
4. Scar formation
- Granul­ation tissue­>Scar
- Composed of inactive spindl­e-s­haped fibrob­lasts, dense collagen, fragments of elastic tissue, ECM
- Pale, avascular
5. Connective tissue remodeling
-Balance between ECM synthesis & degrad­ation
- Degrad­ation of collagen & MMPs > smaller & softer scar

Defective

1.Defe­ctive scar formation
- Ulceration
2.Exce­ssive sf (keloid)
3.Cont­racture
 

Cellular response

important leukocyte; neutrophil and macrop­hages
1. Adhesion to endoth­elium
a. Margin­ation
- stasis of blood >settle out the central flow and marginate along endoth­elium surface
b. Rolling
- comple­mentary surface adhesion molecules sticks and release > rolling along
- mediated by selectins, regulated by cytokines
c. Adhesion
- mediated by intergrins
______­___­___­___­___­___­___­___­___­___­______
2.Migr­ation thru endo
-secrete collag­enase thru basement membrane
- migrate toward chemot­actic gradient
______­___­___­___­___­___­___­___­___­___­______
3.Chem­otaxi
-neutr­oph­il>­mon­ocy­te>­mac­rophage
______­___­___­___­___­___­___­___­___­___­______
4.Phag­ocy­tosis
a. Recogn­ition by receptors to sd signals
b. Activation by cytosolic Ca2+ and enzymes
c. Engulf & Degrad­ation
d. anti-i­nfl­amm­atory effects and wound repair

Morpho­logic patterns and systemic effects

Morpho­logic patterns
Cytoki­ne-­induced systemic reaction aka Acute-­phase responses
1.Serous
1.Fever by pyrogens
2. Fibrinous
2. Leukoc­ytosis
- Increase cell fibrin
3.Phase proteins
- risk of scar formation
- CRP, Fibrin­oge­n,SAA
3.Purulent
-Pus, leukocyte and debris
4. Ulcer
- Open lesion

Possible outcomes

1.Complete resolution
2. Fibros­is/­sca­rring
3.Chronic inflam­mation

Cells and mediators

Macrophage
- dominant, from monocyte
Activated by:
1. Classical pathway (micro­bicidal action)
2. Altern­ative pathway
Functions
1. Phagoc­ytosis and destru­ction
2. Initiate tissue repair & scar formation and fibrosis involv­ement
3. Secrete inflam­mation mediators (e.g. cytokines, clotting factors)
4. Processing and presen­tation of Ag to immune system

Tissue repair -- Regene­ration (Cell prolif­era­tion)

Depend on:
1. Cell types (Ability to repair)
2. Degree of injury
Prolif­erative potential
1. Labile (continuo)
- e.g. epithelial cell, xxx tract
2. Stable
- e.g. salivary gland
3. Permanent
- e.g. neuron, myocardium
 
Regulation mechanism
1. Growth factors (+popu­lat­ion­,si­ze,­mit­osi­s,s­urv­ival)
-VEGF
2. ECM
Cell-m­atrix intera­ctions
總之講緊gr­owth同 differ­ent­iat­ion要用at least 2 types of signal 一個就用so­lub­le(­growth factor) 另一個就用i­nso­lub­le(ECM)

Secondary intention

- Cell loss more extensive
Features
1. More intense inflam­matory tissue
2. Abundant granul­ation tissue
3. ECM accumu­lation
4. Formation of large scar
- Destroyed appendage are perman­ently lost
5. Wound contra­ction
- Reduce gap between dermal edge and wound area to close wound
- Myofib­roblast for mediator
6. Fibrosis
- Excessive collagen deposit
- Pathologic process by persistent stimuli
- Associated with loss of tissue
- Long-l­asting

Healing Factors

Systemic
1. Overall nutrition e.g. VitC
2. Metabolic status > Vascular supply
3. Circul­atory status
4. Hormones > Cortico :(
5. Age
Local
1. Infection
2. Movement
3. Type, size, location
4. Foreign bodies